**6. Methods**

Diffusion (DWI) is the best MRI technique to differentiate ischemia from chronic infarction. While the latter shows an increase in diffusion, the former classically restricts diffusion [65]. The identification of acute lesions in patients with multiple chronic lesions makes DWI a tool

Water in tissues has a randomized translational movement ("Brownian motion") in its molecules caused by thermodynamic energy and the viscosity of the medium. This type of

Diffusion imaging is sensitive to the microscopic movement of water protons. Water protons undergo a change during the transverse magnetization phase in the presence of a magnetic field gradient. Thus, areas with greater diffusion (faster movement) are subject to a high degree of signal attenuation compared with areas with lower diffusion (slow/restricted movement), which show lower signal attenuation. Animals subjected to occlusion of the middle cerebral artery (MCA) showed signs of ischemia in diffusion within 45 minutes. These findings are believed to reflect the restriction of water movement by the cellular membrane. MRI's greater sensitivity for detecting acute ischemia in diffusion is believed to be a result of the movement of water within the cell, which restricts the movement of water protons (cytotoxic edema), while the T2-weighted images show a signal change that results mainly from vasogenic edema. It is estimated that cytotoxic edema begins very soon after ischemic abuse, while the vasogenic

Moseley et al. [65] argued that significant diffusion decrease (restriction or reduction) in ischemia reflects the deviation of an environment with extracellular water protons with a faster diffusion to a more restricted intracellular environment, in addition to the depletion of the sodium-potassium pump in the cellular membrane because of infarction. The cytotoxic edema

Nonetheless, the diffusion of ischemia areas can be reversed after early reperfusion and are potentially reversible if they occur after CAS. It has also been shown that ischemic lesions in

The embolic complications identified in DWI occur more frequently than the apparent low rate of clinical complications would suggest. An MRI may quantify the ischemic foci, making

To examine this issue more deeply, we conducted a prospective randomized study (patients chosen randomly from the outpatient neuroradiology service of INCOR) in a case-control setting [68]. We used angiographic exams and MRI studies that showed cerebral embolism represented by the diffusion sequence (DWI) before and after surgical endovascular treatment to quantify, locate, and measure new restriction foci in diffusion MRI and to correlate the new DWI restriction foci with demographic aspects (gender, age, side of the carotid treated, and symptoms), risk factors for cerebrovascular disease, aspects of the angioplasty technique used,

diffusion might not leave changes that appear in later MRI scans after TIA frames.

it an important method for validating the advantages and complications of CAS.

of unquestionable value in current imaging practice.

156 Carotid Artery Disease - From Bench to Bedside and Beyond

movement is related to CDA, and MRI uses DWI to evaluate it [66,67].

edema begins to develop 6 hours after the ischemic incident.

is thus responsible for reducing diffusion during ischemia.

and the presence of previous infarcts in MRI.

Our sample consisted of 40 patients presenting carotid stenosis of atherosclerotic origin. The patients were referred for MRI exams with diffusion techniques before and after CAS. All of the patients in this prospective study signed an informed consent form. The inclusion criteria were as follows: patients with serious carotid stenosis (shown by Doppler, ATC, or digital subtraction angiography [DSA]) who were referred for endovascular treatment for carotid atheromatous disease according to the local institutional guidelines, who agreed to participate in the research protocol, and who had MRI studies conducted with diffusion techniques at most 24 hours before and up to 72 hours after the CAS with a protection filter.

Exclusion criteria were the following: intra-arterial thrombi observed in the angiography before CAS; patients with disabling complications from previous cerebral infarcts; contrain‐ dications for the MRI scan, such as a cardiac pacemaker or claustrophobia, patients with macroemboli in the DSA after CAS, clinical conditions compatible with ischemia after CAS, angiographic exam showing stenosis <60%, MRI exams with movement artifacts, and imaging studies with serious stenosis in the contralateral cervical carotid, vertebral arteries, or intra‐ cranial arteries.

Three patients out of 40 were excluded because they showed stenosis <60%, and one patient was excluded for having exceeded the maximum time established for MRI after CAS because of coronary angina and hemodynamic instability.

The MRI studies were performed using commercially available single high-field equipment (1.5 T, LX Horizon®, General Electric Healthcare) with a skull coil ("birdcage transmit/receive quadrature").

The MRI scans before and after CAS followed the same sequencing protocol:


New foci (NF) of ischemia were defined as the presence of a hypersignal (restriction) in diffusion after CAS that was not present in the same sequence before CAS. These foci were considered recent, additional infarcts compared with the first MRI.

difficulty of relating the localization of the embolism precisely with the artery that underwent

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The diameter of each NF was noted using the maximum diameter of the lesion in the DWI sequence through a metric analysis determined manually in the software (eFilm®). For comparison, the NFs were divided into three groups of diameters (<5 mm, between 5 and 10 mm and >10 mm) according to the stratification method published by other authors [69,70]. The patients with carotid occlusion contralateral to the CAS were noted. To mark the occlusion of the internal carotid artery, we used DSA or MRI. In the absence of DSA in the carotid artery, we defined occlusion using MRI when there was no "flow-void" phenomenon and a high intravascular signal in the FLAIR sequence, compatible with thrombus in sections focusing on the internal intracranial carotid artery. Both imaging methods were accepted as sufficient for

Areas with DWI restriction after CAS (ischemia indicators) were correlated with demographic aspects, aspects of the angioplasty technique, stenosis characteristics, and the presence of previous infarctions on MRI. The quantification of stenosis in the carotid bulb studied was

The patients were divided into two groups: "brief" angiography and "complete" angiography. An angiographic exam before CAS is conventionally called a brief angiography when the exam only includes an angiography of the carotid artery that is a candidate for treatment. A complete

Antiplatelet therapy was standardized, and all patients received 75 mg clopidogrel and 100 mg acetylsalicylic acid orally on a daily basis, beginning at least five days before the procedure. In the preparation of the materials, all of the introducers, catheters, and sheaths were pre‐ washed with physiologic saline flow and subsequently packed in a sterile container with

Under local anesthesia and light sedation from the anesthesiologist, arterial puncture was performed and the valved introducer was deployed in the common femoral artery, which was fixed to the skin with a wire suture for safety. If there was significant tortuosity of the iliac and femoral vessels, long introducers were sufficient to help stabilize the catheter and the catheter

A bolus injection of 10,000 units of heparin was administered intravenously after the valved introducer was installed. An atropine solution was prepared before the angioplasty and stored until the stent's release. Intermittent verbal communication was maintained with the patient during the procedure by the doctors performing the CAS, as in the eventual clinical tests.

In all cases, the angiography of the carotid artery undergoing CAS was initially performed with a 5 Fr angiographic catheter to confirm the stenosis shown with other methods. At this point in the procedure, angiographies of the cerebral vessels nourished by the carotid artery

angiography includes the study of other cervical arteries or the aortic arch.

angioplasty, we decided not to include these two cases in the analysis of laterality.

proving that a vessel was occluded.

**7. Angioplasty technique used**

guide in the common carotid arteries.

using the NASCET method [10] with DSA in all cases.

physiologic serum and heparin before arterial puncture.

The opposite of a recent infarction caused by DWI after CAS is an old infarction that is present in the T2W sequencing of the MRI before CAS. Chronic cerebral infarction is the end result of prolonged ischemia. Areas of hypersignal in the cerebral parenchyma in the T2 sequence with areas corresponding to the variable signal in T1 (with the tendency to be isointense compared with the fluid in T1 and T2) without restriction in DWI and with no enhancement after paramagnetic contrast were considered old infarctions ("T2W infarction"). Other diseases that may have a signal aspect similar to that of old infarctions (for example: porencephalic cysts, arachnoid cysts, low-grade astrocytoma) were excluded from the count because of their topographic characteristics, their appearance on the edge of the lesion, or their appearance on the surrounding tissue or because they showed a signal that differed from that of the fluid in the other sequences in the MRI study.

The MRI images were analyzed by the consensus of two experienced neuroradiologists using the eFilm® software without access to the clinical data or angiography and CAS data. If there were discrepancies between the two neuroradiologists' findings, the studies were analyzed by a third observer to reach a consensus.

The NF were correlated with age, gender, side of carotid artery treated, presence of previous symptoms related to carotid stenosis, risk factors for atherosclerosis and ICVA (diabetes mellitus, systemic arterial hypertension, hypercholesterolemia, ischemic coronary artery disease, arrhythmia, ischemic peripheral vascular disease, transient ischemic attack [TIA], and ischemic cerebrovascular accident [ICVA]), percentage of carotid stenosis, presence of ulcers in the atheromatous plaque, previous infarction noted on the MRI, number of catheters used, number of arteries on which angiographies were performed, contralateral carotid occlusion, endovascular access technique used to reach the common carotid artery on the side of the angioplasty, type of filter, type of stent, volume of contrast used in the CAS and angiography, fluoroscopy time spent during the procedure, and the localization, number, and diameter of these NF. These parameters were also correlated between patients with only one NF and those with multiple NFs.

The localization (laterality) of the encephalic NF was defined as ipsilateral if it coincided with the area supplied by the carotid artery undergoing angioplasty. The localization of the NF was defined as contralateral if the cerebral area did not coincide with the side of the CAS, meaning the area was nourished by the carotid artery contralateral to the angioplasty or the area located on the posterior fossa. In cases when it was impossible to determine laterality, the patient was excluded from the analysis, which occurred with two patients. Patients 16 and 27 showed stenosis in the carotid artery (left) and contralateral occlusion (right), with NF identified in the area supplied by the right carotid artery. Under this condition, the flow to the carotid area can use the anastomotic Willis polygon or openings in other collateral pathways can be determined (for example: flow through the vasa vasorum or retrograde flow through the ophthalmic artery). Thus, with NF in the area of the occluded artery, it is not possible to say with certainty whether the embolism originated directly in the CAS or migrated through the anastomosis of areas that revascularized the cerebral territory of the occluded carotid artery. Because of the difficulty of relating the localization of the embolism precisely with the artery that underwent angioplasty, we decided not to include these two cases in the analysis of laterality.

The diameter of each NF was noted using the maximum diameter of the lesion in the DWI sequence through a metric analysis determined manually in the software (eFilm®). For comparison, the NFs were divided into three groups of diameters (<5 mm, between 5 and 10 mm and >10 mm) according to the stratification method published by other authors [69,70].

The patients with carotid occlusion contralateral to the CAS were noted. To mark the occlusion of the internal carotid artery, we used DSA or MRI. In the absence of DSA in the carotid artery, we defined occlusion using MRI when there was no "flow-void" phenomenon and a high intravascular signal in the FLAIR sequence, compatible with thrombus in sections focusing on the internal intracranial carotid artery. Both imaging methods were accepted as sufficient for proving that a vessel was occluded.

Areas with DWI restriction after CAS (ischemia indicators) were correlated with demographic aspects, aspects of the angioplasty technique, stenosis characteristics, and the presence of previous infarctions on MRI. The quantification of stenosis in the carotid bulb studied was using the NASCET method [10] with DSA in all cases.
